Researchers develop a caspase inhibitor that only works after being irradiated with UV light, giving them control over apoptosis in human cells.

A new inhibitor gives researchers the ability to control programmed cell death in cultured human T cells.

The Yale neuroscientist seeks to understand the brain’s architecture and function using C. elegans.

Introducing either necroptotic cells or an enzyme that triggers necroptosis can wipe out cancer.

Telomeres in cancer cells exposed to oxidative stress got shorter and stickier.

When hair follicle stem cells lose their protein-based death cue, they take on a new role helping to repair wounds in skin.

Internalizing the environment might be the next step in humans’ relationship with our planet.

Apoptosis and other types of programmed cell death appear to be reversible.

Molecular programs can rescue cells already engaged in the process of apoptosis or other forms of programmed cell death.

The biologist earned a Nobel Prize in 2002 for his work on C. elegans.

M proteins from Streptococcus bacteria selectively kill mouse macrophages and human macrophage-like cells by prompting cell death.

The immune cells—known for clearing dead cells—also chew up live progenitors in neurogenic regions of mouse brains. 

A decade of research on intercellular mitochondrial transfer has answered some long-standing questions and raised new ones.

The tale of p53, a widely studied tumor suppressor gene, illustrates the inventiveness of researchers who turn mishaps into discoveries.

In estrogen receptor–positive breast cancer, the transcription factor IRF1 tips the balance between cellular suicide and survival through autophagy.

In Chapter 12, "Of Mice and Men," author Sue Armstrong recounts the point at which researchers moved from working with p53 in tissue culture to studying the gene in animal models.

Scientists show how cell stress both prevents and promotes cell suicide in a study that’s equally divisive.